ReviewJournal of cardiovascular translational research2025
Reprogramming of Mitochondrial and Cellular Energy Metabolism in Fibroblasts and Cardiomyocytes: Mechanisms and Therapeutic Strategies in Cardiac Fibrosis.
Review in Journal of cardiovascular translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Traditional Chinese Medicine Intervention Based on Metabolic-Epigenetic Axis: Mechanism and Treatment Strategy of Chronic Heart Failure.Biomolecules · 2026Review
- CK2α Deficiency Drives Myocardial Fibrosis via Desmin-Induced Mitochondrial Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting the heart-immune axis after myocardial infarction: from inflammation to immunomodulation.Frontiers in cardiovascular medicine · 2026Review
- Oxidative Stress, Mitochondrial Homeostasis, and Sirtuins in Atrial Fibrillation.International journal of molecular sciences · 2025Review
- Decoding cardiac metabolic reprogramming through single-cell multi-omics: from mechanisms to therapeutic applications.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Cardiac fibrosis, marked by excessive extracellular matrix accumulation, is a key endpoint in various cardiac diseases and is linked to energy metabolic disorders. This review explores the relationship between mitochondrial energy metabolism and cardiac fibrosis, focusing on the metabolic reprogramming in fibroblasts and cardiomyocytes during fibrosis development. We examine changes in substrate utilization, oxidative phosphorylation (OXPHOS), and ATP production that characterize the fibrotic heart. The metabolic dysregulation involves disruptions in fatty acid oxidation, glucose metabolism, and amino acid metabolism, contributing to fibrosis pathogenesis. Additionally, we discuss the implications of these metabolic alterations for therapeutic strategies, highlighting the potential of targeting energy metabolism to reverse or halt cardiac fibrosis progression. By synthesizing current knowledge and identifying research gaps, this review aims to lay the groundwork for future studies and enhance therapeutic approaches for this challenging condition.
Indexed as
Identifiers
40825914What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.